Possible mechanisms of the protection of ginsenoside Re against MPTP-induced apoptosis in substantia nigra neurons of Parkinson's disease mouse model

• Published in: Journal of asian natural products research Vol. 7; no. 3; pp. 215 - 224
• Main Authors: Xu, Bei-Bei, Liu, Chun-Qing, Gao, Xi, Zhang, Wan-Qin, Wang, Shi-Wei, Cao, Ying-Lin
• Format: Journal Article
• Language: English
• Published: Abingdon Taylor & Francis GroupAbingdon, UK 01.06.2005; Taylor & Francis
• Subjects: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Apoptosis; Apoptosis - drug effects; bcl-2-Associated X Protein; Biological and medical sciences; Caspase 3; Caspases - metabolism; General pharmacology; Ginsenoside Re; Ginsenosides - pharmacology; Medical sciences; Mice; Mice, Inbred C57BL; MPTP; Nitric Oxide Synthase - analysis; Nitric Oxide Synthase Type II; Parkinson's disease; Parkinsonian Disorders - drug therapy; Parkinsonian Disorders - metabolism; Parkinsonian Disorders - pathology; Pharmacognosy. Homeopathy. Health food; Pharmacology. Drug treatments; Proto-Oncogene Proteins c-bcl-2 - analysis; Proto-Oncogene Proteins c-bcl-2 - genetics; RNA, Messenger - analysis; Substantia Nigra - drug effects; Substantia Nigra - pathology; Substantia nigra neuron; Steroid; Ginsenoside Re; Parkinson's disease; Rat; Parkinson disease; Saponin; Substantia nigra neuron; Degenerative disease; Glycoside; Mechanism of action; Terpenoid; Nervous system diseases; Rodentia; Neuroprotective agent; Antiparkinson agent; Biological activity; Vertebrata; Experimental disease; Mammalia; Locus niger; Neuron; Cytoprotector; Animal; Central nervous system disease; Triterpene; MPTP; Apoptosis
• ISSN: 1028-6020; 1477-2213
• DOI: 10.1080/10286020410001690172

We have investigated the role of ginsenoside Re (Re) in preventing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced apoptosis of the substantia nigra neurons in the mouse model of Parkinson's disease (PD). C57BL mice have been administrated i.s.c. with MPTP to establish the PD model. Pretreatment groups were given different doses of Re (6.5, 13, 26 mg kg −1 ) i.g. for 13 days. Transmission electron microscope (TEM), tyrosine hydroxythase (TH) immunostaining and TDT-mediated dUTP nick-end labeling (TUNEL) staining have been used to observe the damage of substantia nigral neurons. To measure the expression of inducible nitric oxide synthase (iNOS), Bcl-2, Bax protein and expression of Bcl-2, Bax gene, immunohistochemistry and in situ hybridization have been explored respectively. Western blot analysis has been performed with anti-caspase-3. Pretreatment with Re (13, 26 mg kg −1 ) markedly increases TH-positive neurons and decreases the TUNEL-positive ratio compared with the MPTP model group. Furthermore, Re could enhance the expression of Bcl-2 protein and Bcl-2 mRNA, but reduce the expression of Bax, Bax mRNA, and iNOS, and weaken the cleavage of caspase-3. In summary, ginsenoside Re showed protection from MPTP-induced apoptosis in the PD model mouse nigral neurons and this effect may be attributable to upregulating the expression of Bcl-2 protein, downregulating the expression of Bax, and iNOS protein, and inhibiting the activation of caspase-3.